COVID-19 is a multisystem disease and is associated with significant respiratory distress, systemic hyper inflammation, vasculitis & multi-organ failures. 1/
SARS-CoV-2 causes deterioration of numerous systems with increasing evidence implying that COVID-19 affects endothelium and vascular function. Endothelial dysfunction plays a crucial role in the pathophysiology of SARS-CoV-2. 2/
SARS-CoV-2 causes deterioration of numerous systems with increasing evidence implying that COVID-19 affects endothelium and vascular function. Endothelial dysfunction plays a crucial role in the pathophysiology of SARS-CoV-2. 3/
The Angiopoietin 1/Tie 2 pathway plays an important role in endothelium quiescence and vessel stability. The disruption of Angiopoietins/Tie balance affects vessel contact barrier and leads to vessel leakage, and this in turn causes endothelial dysfunction. 4/
Although vascular instability through SARS-CoV- 2 is associated with endothelial dysfunction, it is still not understood if the virus affects Angiopoietin/Tie axis directly or via other mechanisms such as cytokine storm and/or immune response associated with the infection. 5/
It is also possible that SARS-CoV-2 may indirectly affect Angpt/Tie 2 signalling through inflammatory cytokine storm & stimulation of a pro-thrombotic state. 6/
Inflammatory cytokines such as TNF-α and IL-6 upregulate Angpt 2 by inhibition of nitric oxides and NFκB activation, and thus suppress Angpt 1/Tie 2 signalling. 7/
Direct endothelial virus infection or infection of neighbouring cells may cause disruption of Angpt 1/Tie 2 and endothelial dysfunction during the immune activation against infection. 8/
As previously mentioned, SARS-CoV-2 is associated w/ long term vascular pathology & endothelial injury. Therefore, more research is required in order to understand molecular impact SARS-2 has on endothelial dysfunction & Angiopoietin/Tie axis to improve treatment and care 9/
A new review provides an overview of the impact SARS-CoV- 2 has on endothelial function and more specifically the Angiopoietin/Tie pathway. 10/10
preprints.org
preprints.org
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